31, p = 0.43). The arithmetic sum of all the 13 gluEPSPs shown in Figure 7B is 6.1 mV (see Figures 7C and 7D). Assuming the dendritic membrane potential ABT-263 concentration to be −86 mV this would correspond to a dendritic peak depolarization to −35 mV. The depolarization
by the average single gluEPSP of 0.48 mV at the soma corresponds to a dendritic depolarization to −82 mV. Assuming a synaptic reversal potential of 0 mV the loss of driving force is around 60%. Thus, the expected linear sum gluEPSP at the soma corrected for driving force loss is just 2.6 mV. Data analysis was performed using Igor Pro (Wavemetrics). Distance measurements were performed on image stacks collected at the end of recordings learn more using ImageJ (NIH). The distance between the soma and the input site was measured from the center of the soma to the approximate midpoint of the input site in the case of gluEPSPs evoked by multisite uncaging. Distances in double-patch and modeling experiments are Euclidean distances. All values are given as
mean ± standard error of mean unless otherwise noted. This work was supported by the Deutsche Forschungsgemeinschaft (SFB TR3), Nationales Genomforschungsnetzwerk NGFNplus EmiNet, EPICURE, ERANET Neuron ‘EpiNet’, Ministry for Innovation, Research, Science, Research, and Technology NRW, and the BONFOR program of the University of Bonn Medical Center. We thank J.C. Magee and D. Dietrich for suggestions on the manuscript, T. Nevian for technical help with Phosphoprotein phosphatase the dendritic recordings, and F. Helmchen for support. “
“Abrupt changes in an organism’s environment precipitate requisite and rapid adaptive changes in neural circuits. In particular, synapses in hypothalamic nuclei that form the neural network underlying energy balance and food intake are remarkably
susceptible to variations in the availability of food. The dearth of food is of such importance to an organism that it triggers both direct changes in food-related signals and the immediate activation of the stress response that increases circulating corticosteroids (CORT) (Bligh et al., 1990, Dallman et al., 1999 and McGhee et al., 2009). The dorsomedial nucleus of the hypothalamus (DMH) regulates food intake and serves as a center for the integration of food and stress signals (Bellinger and Bernardis, 2002 and DiMicco et al., 2002). More recently, the DMH has also been implicated as being the key food entrainable oscillator in the brain that exhibits synchronous activity in response to food deprivation (Gooley et al., 2006 and Mieda et al., 2006). Although both of these roles are key to an organism’s survival, surprisingly little is known about synaptic processing in the DMH and even less is known about the effects of food deprivation on synaptic function and plasticity in this nucleus.